1 CHO cells expressing the a 1C-a subunit (cardiac isoform) and the a 1C-b subunit (vascular isoform) of the voltage-dependent L-type Ca 2+ channel were used to investigate whether tissue selectivity of Ca 2+ channel blockers could be related to di erent a nities for a 1C isoforms. 2 Inward current evoked by the transfected a 1 subunit was recorded by the patch-clamp technique in the whole-cell con®guration. 3 Neutral dihydropyridines (nifedipine, nisoldipine, (+)-PN200-110) were more potent inhibitors of a 1C-bsubunit than of a 1C-a -subunit. This di erence was more marked at a holding potential of 7100 mV than at 750 mV. SDZ 207-180 (an ionized dihydropyridine) exhibited the same potency on the two isoforms. 4 Pinaverium (ionized non-dihydropyridine derivative) was 2 and 4 fold more potent on a 1C-a than on a 1C-b subunit at Vh of 7100 mV and 750 mV, respectively. E ects of verapamil were identical on the two isoforms at both voltages. 5 [ 3 H]-(+)-PN 200-110 binding experiments showed that neutral dihydropyridines had a higher a nity for the a 1C-b than for the a 1C-a subunit. SDZ 207-180 had the same a nity for the two isoforms and pinaverium had a higher a nity for the a 1C-a subunit than for the a 1C-b subunit. 6 These results indicate marked di erences among Ca 2+ channel blockers in their selectivity for the a 1C-a and a 1C-b subunits of the Ca 2+ channel.

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On isolated hearts obtained from control rats and rats subjected to regular physical exercises (forced swimming) during 6 weeks, we studied the contractile activity of the heart, resistance of the myocardium to ischemia/reperfusion-induced injuries, as well as the dependence of the developed and end-diastolic pressures in the aortic ventricle (AV) on the strain of the myocardium (by means of a dosed increase in the volume of a polyethylene reservoir inserted into the ventricle). It was demonstrated that adaptation to regular graduated physical exercises exerts a positive effect on the functional state of the AV myocardium and its contractile function. This was manifested in intensification of the contractile activity of the myocardium, a decrease in its oxygen "job cost," and an increase in the resistance to injuries induced by ischemia-reperfusion. In addition, regular physical trainings led to an increase in the resistance of the AV myocardium to the strain. In trained rats, the plateau of the Frank-Starling plot was significantly greater than that in control animals, while the rigidity of the AV myocardium was significantly lower.